Evidence map›Paper›PMID 37638180›Full record

ReviewFrontiers in neurology2023

Traumatic brain injury and the pathways to cerebral tau accumulation.

William P Flavin, Helia Hosseini, Jeffrey W Ruberti, H Pirouz Kavehpour, Christopher C Giza, Mayumi L Prins

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  2. Article
  3. Bioenergetics of the combat sports brain: Between risk and resilience.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Targeting dual specificity tyrosine-phosphorylation-regulated kinase 1A mitigates tauopathy and enhances recovery after repetitive head injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Observational
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

William P FlavinDepartment of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States.
Helia HosseiniDepartment of Bioengineering, UCLA, Los Angeles, CA, United States.
Jeffrey W RubertiDepartment of Bioengineering, Northeastern University, Boston, MA, United States.
H Pirouz KavehpourDepartment of Bioengineering, UCLA, Los Angeles, CA, United States.
Christopher C GizaSteve Tisch BrainSPORT Program, Department of Pediatrics and Neurosurgery, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States.
Mayumi L PrinsSteve Tisch BrainSPORT Program, Department of Pediatrics and Neurosurgery, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States.
University of California, Los Angeles · USLa Jolla Bioengineering Institute · USNortheastern University · US

Funding

Translational Neuroscience Training GrantR25NS065723 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARMICHAEL, STANLEY THOMAS · 2009 to 2023
$2.8M
UCLA Neuroscience Physician-Scientist Training ProgramUE5NS065723 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Stanley Thomas Carmichael, Jason D Hinman · 2024 to 2026
$1.2M
NINDS NIH HHS R25 NS065723NINDS NIH HHS UE5 NS065723
6 · The paper itself

Abstract

Tau is a protein that has received national mainstream recognition for its potential negative impact to the brain. This review succinctly provides information on the structure of tau and its normal physiological functions, including in hibernation and changes throughout the estrus cycle. There are many pathways involved in phosphorylating tau including diabetes, stroke, Alzheimer's disease (AD), brain injury, aging, and drug use. The common mechanisms for these processes are put into context with changes observed in mild and repetitive mild traumatic brain injury (TBI). The phosphorylation of tau is a part of the progression to pathology, but the ability for tau to aggregate and propagate is also addressed. Summarizing both the functional and dysfunctional roles of tau can help advance our understanding of this complex protein, improve our care for individuals with a history of TBI, and lead to development of therapeutic interventions to prevent or reverse tau-mediated neurodegeneration.

Indexed as

brain pathologyneurodegenerationrepetitive head injurytautraumatic brain injury

Identifiers

PMID37638180
PMCPMC10450935
OpenAlexW4385759467

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.